Endothelial Regulation of Vascular Tone and Growth

Abstract

The endothelium regulates vascular tone by releasing factors involved in relaxation and contraction, in coagulation and thrombus formation, and in growth inhibition and stimulation. Endothelium-dependent relaxations are elicited by transmitters, hormones, platelet substances, and the coagulation system, and by physical stimuli such as the shear stress from circulating blood. They are mediated by the endothelium-derived relaxing factor, recently identified as nitric oxide, which causes vasodilation and platelet deactivation. Other proposed endothelium-derived relaxing factors include a hyperpolarizing factor, lipooxygenase products, and the cytochrome P450 pathway. Endothelium-derived contracting factors are produced by the cyclooxygenase pathway and by endothelial cells, which produce the peptide endothelin-1, a potent vasoconstrictor that under normal conditions circulates at low levels. The endothelium produces both growth inhibitors-normally dominant-and growth stimuli. Denuded or dysfunctional endothelium leads to a proliferative response and intimal hyperplasia in the vessel wall; moreover, platelets adhere to the site and release potent growth factors. Endothelial dysfunction has numerous causes: Aging is associated with increased formation of contracting factor and decreased relaxing factor; denudation, such as by coronary angioplasty, impairs the capacities of regenerated endothelial cells; oxidized low-density lipoproteins and hypercholesterolemia interfere with nitric oxide production; hypertension morphologically and functionally alters the endothelium; and atherosclerosis markedly attenuates some endothelium-dependent relaxations. For patients with coronary bypass grafts, differences in endotheliumderived vasoactive factors between the internal mammary artery and the saphenous vein may be important determinants of graft function, with the mammary artery having more pronounced relaxations than the saphenous vein and thus a higher patency rate. Am J Hypertens 1993;6:283S-293S KEY WORDS: Endothelial regulation, endothelial dysfunction, vascular tone, endothelium-derived relaxing factors, endothelium-derived contracting factors, nitric oxide.T he endothelium takes part in the regulation of vascular tone 1 by releasing relaxing and contracting factors both under basal conditions and when activated by neurotransmitters, hormones, autacoids, or physical stimuli. In addition, endothelial cells release factors involved in coagulation and thrombus formation and in growth inhibition and stimulation.Owing to its strategic anatomic position, the endothelium is a target organ for hypertension, diabetes, and hyperlipidemia. 1 Alterations in endothelial function may contribute to the pathogenesis as well as to the progression and complications of hypertension and its sequelae such as atherosclerotic vascular disease. ENDOTHELIUM-DEPENDENT REGULATION OF VASCULAR TONERelaxing Factors Endothelium-dependent relaxa tions occur both in vitro and in vivo 2^; transmitters, hormones, substances derived from platelets, and t...

Alterações vasculares em ratos obesos por dieta rica em gordura: papel da Via L-arginina/NO Endotelial

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Effects of cisplatin on the contractile function of thoracic aorta of Sprague-Dawley rats

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Endothelium-Dependent Regulation of the Cardiovascular System.

“…The promotors include basic fibroblast growth factor, platelet-derived growth factor and possibly also endothelin (89). The inhibitory factors include heparin/heparan sulfate proteoglycans, transforming growth factor-p, and most likely NO (90). Elevation of cyclic GMPlevels in smooth muscle cells is a commonfinal mechanism of actions of nitrovasodilators, including NO (90).…”

“…The inhibitory factors include heparin/heparan sulfate proteoglycans, transforming growth factor-p, and most likely NO (90). Elevation of cyclic GMPlevels in smooth muscle cells is a commonfinal mechanism of actions of nitrovasodilators, including NO (90). Thus, EDRF/NO may help to inhibit growth of smooth muscle cells even atphysiological concentration (88,91).…”